@article{lee_rodriguez_majumdar_de marval_rodriguez-puebla_2021, title={CDK4 has the ability to regulate Aurora B and Cenpp expression in mouse keratinocytes}, volume={22}, ISSN={["1792-1082"]}, DOI={10.3892/ol.2021.12993}, abstractNote={Cyclin-dependent kinase 4 (CDK4) is a critical molecule that regulates key aspects of cell proliferation through phosphorylation of the retinoblastoma (Rb) family of proteins. In the last few years, it has been suggested that CDK4 plays alternative roles in cell proliferation and tumorigenesis. The main aim of the present study was to define a novel CDK4 function as a transcriptional regulator of genes involved in chromosome segregation, contributing to the G2/M phase transition. Herein, chromatin-immunoprecipitation reverse transcription-quantitative PCR assays were performed to demonstrate that CDK4 could occupy the promoter region of genes associated with chromosomal segregation, such as Aurora-B (Aurkb) and Centromere Protein P (CENP-P). Moreover, gain- and loss-of-function experiments showed that CDK4 participated in the transcriptional regulation of Aurkb and CENP-P. The finding that Aurkb may have a crucial role in chromosome bi-orientation and the spindle assembly checkpoint, and that CENP-P could be required for proper kinetochore function suggests that dysregulation of CDK4 expression induces chromosomal instability and, in some cases, cancer development.}, number={4}, journal={ONCOLOGY LETTERS}, author={Lee, Sung Hyun and Rodriguez, Liliana R. L. and Majumdar, Rima and De Marval, Paula L. Miliani and Rodriguez-Puebla, Marcelo L.}, year={2021}, month={Oct} }
 @article{lee_rodriguez_marval_rodriguez-puebla_2020, title={Emergent functions of cyclin-dependent kinase 4 regulating aurora b and cenpp transcription}, volume={80}, ISBN={1538-7445}, DOI={10.1158/1538-7445.AM2020-5814}, abstractNote={Abstract}, number={16}, journal={CANCER RESEARCH}, author={Lee, Sung Hyun and Rodriguez, Liliana R. and Marval, Paula L. Miliani and Rodriguez-Puebla, Marcelo L.}, year={2020}, month={Aug} }
 @article{lee_wang_kim_kim_rodriguez-puebla_2017, title={Cyclin D3 deficiency inhibits skin tumor development, but does not affect normal keratinocyte proliferation}, volume={14}, ISSN={["1792-1082"]}, DOI={10.3892/ol.2017.6551}, abstractNote={Rearrangement and amplification of the D-type cyclin genes have been reported in human cancer. Previous studies have demonstrated that Ras-mediated skin tumorigenesis depends on pathways that act through cyclin D1 and D2; however, the role of cyclin D3 remains unknown. The present study demonstrates that cyclin D3 ablation does not affect keratinocyte proliferation, but instead increases apoptosis levels in the bulge region of the hair follicle. Consequently, cyclin D3 ablation reduces skin papilloma development in a Ras-dependent carcinogenesis model. Previous results revealed that cyclin D3 preferentially binds to cyclin-dependent kinase 6 (CDK6) in mouse keratinocytes and transgenic expression of CDK6 (K5CDK6 mice) inhibits skin tumor development. Thus, we hypothesized that the inhibitory effect of CDK6 is dependent on cyclin D3 expression. To test this hypothesis, a mouse model that overexpresses CDK6 and does not express cyclin D3 (K5CDK6/cyclin D3-/− compound mouse) was developed. Biochemical analysis of the epidermis of K5CDK6/cyclin D3-/− mice revealed that cyclin D3 ablation resulted in increased expression of cyclin D1 protein, with a consequent elevation in the level of CDK6/cyclin D1 and CDK4/cyclin D1 complexes. These findings were concurrent with the increase skin papilloma malignant progression observed in K5CDK6/cyclin D3-/− mice. In summary the absence of cyclin D3 led to fewer number of papillomas in cyclin D3-ablated mice than in the wild-type owing to increased apoptosis, suggesting that alterations in cell survival are a crucial mechanism for crippling cellular defense against neoplasia. The results of the current study also suggest that although cyclin D3 expression does not alter the tumor suppressive role of CDK6 in skin carcinogenesis, the compensatory increase in cyclin D1 can shift the balance towards malignant progression.}, number={3}, journal={ONCOLOGY LETTERS}, author={Lee, Sung Hyun and Wang, Xian and Kim, Sun Hye and Kim, Yongbaek and Rodriguez-Puebla, Marcelo L.}, year={2017}, month={Sep}, pages={2723–2734} }
 @article{lee_hyun_2013, title={Evaluation of 3-methylhistidine levels in dogs with chronic mitral valve disease}, volume={172}, number={16}, journal={Veterinary Record}, author={Lee, S. G. and Hyun, C.}, year={2013}, pages={426-} }